Journal of Nutrition最新文献

Plant-derived glycoproteins and arabinogalactan proteins (AGPs) are increasingly recognized for their multifunctional bioactivity and relevance to food, health, and biotechnology. Present across botanically diverse species and environmental contexts, AGPs exhibit a wide range of physiological effects, including immunomodulatory, anti-inflammatory, antioxidant, antihyperglycemic, antiproliferative, and antiallergenic activities. This review offers a comprehensive overview of the therapeutic and nutritional potential of AGPs, emphasizing their structural diversity and emerging role as bioactive components in functional foods. Special focus is placed on their mechanisms of action and potential applications in nutraceuticals and biotechnological innovations. By summarizing current findings, the review highlights future research directions for exploiting AGPs as valuable yet underexplored, plant-derived ingredients in health-oriented food development.

Background: Habitual dairy consumption reduces risk factors for obesity and its associated characteristics of the metabolic syndrome.

Objectives: This study aims to describe the effect of adding 3 daily servings of full-fat dairy to the diet of adults with overweight and obesity, counseled to follow Canada's Food Guide (CFG).

Methods: A 12-wk single-blinded, parallel, randomized study was conducted in 74 participants [age: 36.55 ± 1.04 y; body mass index (BMI): 29.34 ± 0.43 kg/m²] assigned to 1 of 3 groups: 1) low dairy energy restriction (LD-ER): 500 kcal restriction with ≤1 serving of low-fat dairy, 2) 3 dairy energy neutral (3D-EN): 500 kcal restriction replaced by 3 servings of full-fat dairy, and 3) 3 dairy ad libitum (3D-AL): no energy restriction with 3 servings of full-fat dairy. Changes in physiological outcomes and dietary intakes were measured over 12 wk.

Results: Body weight and BMI were reduced by treatment (P < 0.05) in LD-ER over the 12 wk (P > 0.05). In 3D-AL, a decrease (0.25 ± 0.34 cm) in hip circumference (P < 0.05) and in systolic blood pressure (2.72 ± 2.18; P < 0.05; SBP) was found at week 12. SBP also decreased in LD-ER (P < 0.05). Triglycerides increased in all groups at week 4 (P < 0.05) but returned to baseline by week 12. Neither treatment nor time affected waist circumference, fat and fat-free mass, resting metabolic rate, fasting blood cholesterol, and urine creatinine and urea (P > 0.05). Protein and calcium (P < 0.04) intakes were increased with time in 3D-EN and 3D-AL but not in LD-ER. Compliance with CFG, assessed by a food tracker, increased with time (77% by week 12).

Conclusions: Frequent and daily consumption of full-fat dairy as part of a healthy diet is consistent with CFG. This study was registered at clinicaltrials.gov as NCT04399460 on 22 May, 2020 (https://www.

Clinicaltrials: gov/study/NCT04399460).

Background: Ultraprocessed food (UPF) intake is associated with increased type 2 diabetes (T2D) risk. No controlled feeding trial has investigated UPF exposure and T2D risk or performed chemical analysis of UPF study diets.

Objectives: To design and chemically validate nutritionally matched high- and non-UPF diets and to examine the effects of a 6-wk high-UPF diet on T2D risk in midlife adults.

Methods: High-UPF (81% UPF energy) and non-UPF (0% UPF energy) diets were designed and chemically analyzed to validate energy, macro- and micronutrients, and other dietary components. Plant-based ingredients in the diet were also assessed by FoodSeq. After a 2-wk standardized lead-in diet (58% UPF), 18 adults aged 40 to 65 y were randomly assigned to a eucaloric high-UPF or non-UPF diet for 6 wk. Insulin sensitivity and 24-h glycemic control were measured at baseline and post intervention. Serum global metabolomic profiles were evaluated.

Results: The high-UPF and non-UPF diets were well-matched and consistent with planned energy and nutrient targets. FoodSeq indicated that the high-UPF diet showed more frequent detection of UPF ingredients, such as guar (gum) and corn (corn starch and corn meal). There were no changes in Matsuda Index or HOMA-IR in the pilot trial, however glucose AUC (high-UPF: 13431 ± 3914 mg·min/dL to 13656 ± 4005 mg·min/dL; non-UPF: 15349 ± 4068 mg·min/dL to 14,221 ± 3722 mg·min/dL, P = 0.054; ES = 0.52) and mean amplitude of glycemic excursions (MAGE) (high-UPF: 37.6 ± 10.1 mg/dL to 40.2 ± 7.3 mg/dL; non-UPF: 44.5 ± 11.0 mg/dL to 39.3 ± 9.5mg/dL, P = 0.055; ES = 0.51) tended to worsen in the high-UPF vs non-UPF groups. In the non-UPF group, reductions in the food contact chemical 2,4-ditert-butylphenol and in the thermal food processing by-product N6-carboxymethyllysine were observed.

Conclusions: Findings provide preliminary evidence that reducing UPF may reduce T2D risk. Large-scale trials are warranted to evaluate causal effects.

Background: Although ∼12% of infants in the United States are fed soy protein-based infant formulas (SF), data on the long-term health effects compared with cow milk-based infant formulas (MF) and human milk (HM) remain limited.

Objectives: This study aims to assess whether SF feeding during infancy influences adolescent growth, adiposity, dietary intake, metabolic health, or pubertal development compared with MF or HM feeding during infancy.

Methods: In the Beginnings follow-up study, 190 participants (SF = 52, HM = 76, MF = 62) were assessed at age 14 y for anthropometry, body composition, dietary intake, cardiometabolic biomarkers, pubertal stage, and reproductive organ volumes and characteristics. Statistical analyses were performed using R (version 4.4.2), and included generalized linear regression models adjusted for age, sex, race/ethnicity, mother's education, and birth characteristics.

Results: At 14.10 ± 0.26 (13.47-14.96) y, adjusted models showed that adolescents who were fed SF as infants had similar body weight, BMI-for-age z-score, fat mass index, abdominal adiposity (visceral and subcutaneous adipose tissue areas), and waist circumference compared with participants fed MF and HM as infants. Energy intake, macronutrient intakes, and diet quality (Healthy Eating Index-2020) were comparable across groups, except for a lower fat intake (%kcal) for participants fed SF and HM as infants compared with MF. There were no significant differences between the groups in blood pressure, glucose metabolism, lipid profile, inflammatory biomarkers, pubertal stage, age of menarche and reproductive organ sizes and characteristics at age 14 y. The prevalence of cardiometabolic risk factors was significantly higher in participants who were fed MF (8.1%) compared with SF (3.8%) and HM (0.0%) as infants.

Conclusions: SF feeding during infancy was associated with similar growth, body composition, cardiometabolic health and puberty outcomes at age 14 y as MF and HM feeding. In adjusted models, HM feeding was protective against adolescent adiposity compared with MF feeding. This study was registered at www.

Clinicaltrials: gov as NCT00616395.

Background: Postprandial elevation of triacylglycerol (TAG) is associated with endothelial dysfunction and represents an important independent cardiovascular disease (CVD) risk factor in women. Although daily intakes of pomegranate seed oil (PSO, 80% conjugated α-linolenic acids) reduce fasting lipids, little is known about the acute effects on postprandial CVD risk markers.

Objectives: This study compared the impact of a PSO-rich meal with those of a control meal on postprandial TAG (primary outcome measure), lipids, glucose, insulin, microvascular function, and cell adhesion molecule responses in postmenopausal women.

Methods: In a single-blind, randomized controlled postprandial crossover study, 16 postmenopausal women aged ≤65 y were assigned to consume either a PSO-rich or a control meal on 2 separate occasions, 4 to 6 wk apart. A high-fat mixed meal (50 g fat) was provided at breakfast (0 min), and blood samples collected until 480 min postprandially to assess CVD risk markers. Specific time points were selected for blood pressure (BP) (0, 120, 240, 360 and 480 min) and microvascular reactivity (0, 180, 300, and 420 min). Postprandial data were analyzed using linear mixed models.

Results: Compared with the control meal, the PSO-rich meal significantly reduced the postprandial TAG response but glucose, insulin, apolipoprotein B, and nonesterified fatty acid responses were similar. The AUC and incremental AUC (iAUC) for the postprandial acetylcholine (endothelium-dependent vasodilation) induced reactivity response were greater (P ≤ 0.04), and systolic BP lower after the PSO-rich meal than the control meal. Additionally, the iAUC for the pulse wave velocity and AUC/iAUC for the soluble intercellular adhesion molecule-1 responses were lower, whereas plasma nitrite concentrations were higher after the PSO-rich than control meal (P ≤ 0.037).

Conclusions: A PSO-rich meal significantly reduced the postprandial TAG response and enhanced endothelial function compared with a control meal, suggesting a potential cardioprotective effect in postmenopausal women. This study was registered at clinicaltrials.gov as NCT06042673 (https://clinicaltrials.gov/study/NCT06042673).

Background: Oxytocin (OXT) signaling through the oxytocin receptor (OXTR) produces stress-relieving effects and modulates alcohol reward and sucrose preference in animal models. These findings suggest the therapeutic potential of OXT for alcohol use disorder (AUD) and liver steatosis. However, human genetic evidence linking OXT signaling to these cravings remains scarce.

Objectives: This study examined the association between the OXTR rs53576 polymorphism and habitual intake of alcohol and sucrose in a general population, with a further focus on related liver pathology.

Methods: A cross-sectional analysis was conducted using data from the Shika study, comprising 696 participants with complete information on both single-nucleotide polymorphisms (SNPs) and dietary intake, assessed using the Brief Dietary History Questionnaire (BDHQ). We examined the association of the rs53576 SNP with alcohol and sucrose consumption, as well as with clinical outcomes related to these dietary factors, including liver enzyme concentrations and liver steatosis.

Results: Among individuals with regular alcohol consumption, those with the rs53576 G/G genotype (under a recessive model) exhibited significantly lower alcohol intake (P = 0.002) and higher sucrose intake (P = 0.004) compared with A allele carriers. An association between rs53576 and aspartate aminotransferase (AST) levels, an indicator of alcoholic liver disease (ALD), further supported the relationship between this genotype and alcohol intake. Sex-stratified analysis revealed that the G/G genotype was linked to a greater prevalence of liver steatosis in women, but not in men. Mediation analysis indicated that this association in women was driven by a direct effect independent of sucrose intake volume.

Conclusions: These findings indicate that the OXTR rs53576 polymorphism is associated with distinct alcohol and sucrose intake patterns and susceptibility to liver steatosis, supporting the potential for genotype-informed nutritional interventions aimed at reducing the risk of AUD, ALD, and metabolic dysfunction-associated steatotic liver disease.

Women of reproductive age who suffer from polycystic ovarian syndrome (PCOS), a common and complex endocrine-metabolic illness, are characterized by hyperandrogenism, anovulation, insulin resistance, and persistent inflammation. Its multifaceted etiology includes psychological, environmental, genetic, and epigenetic variables. The potential of nutrigenomics in individualized treatment techniques is highlighted by new research that implicates gene-diet interactions in modifying PCOS susceptibility, phenotypic expression, and therapeutic results. Numerous gene polymorphisms, including those involving the fat mass and obesity-associated gene, methylenetetrahydrofolate reductase, and transcription factor 7-like 2, have been linked to insulin signaling, metabolic disorders, obesity risk, and hormonal imbalances in PCOS. At the same time, dietary bioactives such as flavonoids, omega-3 fatty acids, and folate have demonstrated anti-inflammatory, insulin-sensitizing, and epigenetic-modulating properties, suggesting that they may be utilized to target gene-nutrient interactions and mitigate illness. In order to maximize individualized nutritional therapy for PCOS, this review seeks to investigate integrative nutrigenomics approaches that incorporate dietary interventions with genetic profiling. The review offers a thorough synthesis of recent research by investigating the molecular mechanisms by which gene variations interact with functional nutrition. It determines possible nutraceutical targets for customized treatment. Additionally, the translational significance of these integrative methods is examined in enhancing precision nutrition in PCOS therapy, lowering metabolic risks, and improving clinical outcomes. However, this review underlines the need for an interdisciplinary approach that combines genetics, nutritional science, and clinical practice to promote evidence-based, patient-centric medications for PCOS.

Background: Vitamin B-12 is a cofactor in folate-mediated 1-carbon metabolism, which generates nucleotides {thymidylate [deoxythymidine monophosphate (dTMP)] and purines} and methionine. Depressed de novo thymidylate (dTMP) synthesis leads to uracil accumulation in DNA.

Objectives: This study aimed to determine how B-12 availability affects mitochondrial DNA (mtDNA) integrity and mitochondrial function in skeletal muscle. B-12 deficiency was modeled in young-adult mice. Intramuscular B-12 injection in aged mice assessed the role of B-12 supplementation in age-related changes in skeletal muscle.

Methods: Male methionine synthase knockdown (Mtr^+/-) and wild-type littermates (Mtr^+/+) were weaned to either an AIN93G-based control diet containing 25 μg/kg vitamin B-12 (Mtr^+/+, n = 8; Mtr^+/-, n = 9) or a B-12-deficient (-B-12) diet containing 0 μg/kg vitamin B-12 (n = 9 per genotype) for 7 wk. Aged (20-22 mo) male C57BL/6N mice were acclimated to an AIN93G control diet 4 wk, then received either weekly injections of saline [vehicle control (30 μL 0.9% NaCl; n = 5) or B-12 (0.65 μg per 30 μL 0.9% NaCl; n = 6) in each of 2 hindleg muscles (1.25 μg B-12 total)] for 8 wk. Outcomes measured included maximal oxygen consumption rate, uracil in mtDNA (a biomarker of mtDNA integrity), mtDNA copy number, and mitochondrial mass. Data were analyzed using a 2-way analysis of variance in the Mtr^+/- mouse model exposed to -B-12 diets and by a Student's t-test for B-12 supplementation in aged mice.

Results: The tibialis anterior (TA) muscle from Mtr^+/- mice exhibited 50% lower (P = 0.01) maximal respiratory capacity of the electron transport chain than did TA from Mtr^+/+ mice. Exposure to the -B-12 diet lowered the maximal capacity of complex I in mitochondrially rich muscle (soleus and mitochondria-rich portions of quadriceps and gastrocnemius) by 25% (P = 0.02). Uracil in mtDNA in red muscle and gastrocnemius was elevated ∼10 fold with exposure to -B-12 diet (P = 0.04 and P < 0.001, respectively). In aged mice, gastrocnemius complex IV activity was increased 2-fold with intramuscular B-12 supplementation (P = 0.04).

Conclusions: Exposure to a-B-12 diet led to uracil accumulation in mtDNA and impaired maximal oxidative capacity in skeletal muscle. B-12 supplementation improved complex IV maximal capacity in gastrocnemius from aged mice, a model of age-related skeletal muscle decline.

Background: Genome-wide association studies (GWAS) have identified single-nucleotide polymorphisms (SNPs) associated with perception to sweet taste. The influence of genetic predisposition to sweet taste on diet quality remains poorly understood.

Objectives: This study aimed to compare cross-sectional associations between a genetically driven sweet taste polygenic score (PGS) and alignment with diet quality indices in a cohort of Puerto Rican older adults residing in the Boston area.

Methods: We used baseline data from Boston Puerto Rican Health Study participants with complete genetic and dietary data (n = 583). A weighted sweet taste PGS was constructed using 38 SNPs from published GWAS with perceived intensity sweet taste outcomes (aspartame, fructose, glucose, neohespedirin dihydrochalcone, sucrose, and sweet substances). We derived 3 diet quality indices using data from a food frequency questionnaire validated for this population: Alternate Healthy Eating Index-2010 (AHEI-2010), Dietary Approaches to Stop Hypertension (DASH), and Mediterranean diet (MeD). Multiple linear regression models between sweet taste PGS and diet quality indices were used to estimate associations and 95% confidence intervals (CIs).

Results: There were 428 females and 155 males, with mean age 52.2 ± 7.5 y. The PGS ranged from 30.0 to 50.1, mean (SD): 39.9 (3.4). There was an inverse association between PGS and DASH: β (95% CI) -0.03 [-0.05, -0.004, false discovery rate (FDR) = 0.06], but no association was observed with AHEI-2010: -0.02 (-0.04, 0.008), FDR = 0.19; or MeD: -0.02 (-0.04, 0.01), FDR = 0.19. Across all diet quality indices, higher sweet taste PGS was associated with lower alignment to recommendations for whole grain and vegetables. It also tended to be associated with lower intake of nuts/legumes in the AHEI-2010.

Conclusions: In Puerto Rican adults, higher sweet taste PGS was associated with lower DASH diet quality, but not the AHEI-2010, or MeD, and with lower intake of whole grains, vegetables, and possibly, nuts/legumes. More research is needed on taste perception and dietary intake across populations to inform future intervention.

Background: Diabetic peripheral neuropathy (DPN) is the most common complication of type 2 diabetes mellitus (T2DM) and is associated with substantial morbidity, mortality, and healthcare costs. Vitamin B-12 plays a critical role in nerve protection and regeneration. However, clinical evidence regarding the effectiveness and optimal dose of vitamin B-12 supplementation for managing DPN in individuals with low serum vitamin B-12 levels remains inconclusive.

Objectives: The aim of this study is to compare the effects of 2 different daily doses of oral vitamin B-12 supplementation on neuropathic parameters in patients with DPN and low serum vitamin B-12.

Methods: This 16 wk, randomized controlled trial enrolled adults with T2DM, DPN, and low serum vitamin B12 levels (<200 pg/mL). Patients were randomly assigned (1:1) to receive either 1000 μg or 2000 μg of oral vitamin B12 (methylcobalamin) daily. The primary outcomes were changes in neuropathic parameters, assessed by the numerical rating scale (NRS), Michigan neuropathy screening instrument examination (MNSIE), and neuropathy disability score (NDS). Secondary outcomes included serum B-12 levels and metabolic parameters.

Results: Of the 35 participants randomly assigned, 32 completed the 16-wk trial. Serum vitamin B-12 levels increased significantly in both groups, with a greater rise noted in the 2000 μg group (P = 0.049). Both the 1000 μg and 2000 μg groups experienced significant improvements in neuropathy symptoms. Mean ± SD NRS scores decreased from 7.00 ± 2.03 to 5.60 ± 2.19 (P = 0.016) in the 1000 μg group, and from 6.18 ± 2.40 to 4.42 ± 2.50 (P = 0.007) in the 2000 μg group. Similarly, MNSIE scores improved from 5.70 ± 1.66 to 5.22 ± 1.99 (P = 0.033) and from 5.40 ± 1.68 to 4.47 ± 2.25 (P = 0.022), respectively. No significant difference in these neuropathic outcomes was observed between groups. The NDS remained unchanged in both groups (P > 0.05). In addition, the 1000 μg dose was associated with significant improvements in hemoglobin A1c levels, whereas the 2000 μg dose was linked to a significant decline in estimated glomerular filtration rate.

Conclusions: In patients with DPN and low serum vitamin B-12 levels, 16 wk of daily supplementation with either 1000 μg or 2000 μg of vitamin B-12 similarly improves neuropathic symptoms. Apart from higher serum B-12 levels, the 2000 μg dose did not offer additional neuropathic or metabolic benefits.